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Histopathological Diagnosis of Japanese Spotted Fever Using CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Connector ORIGINAL ARTICLE BACTERIOLOGY Histopathological diagnosis of Japanese spotted fever using formalin- fixed, paraffin-embedded skin biopsy specimens Usefulness of immunohistochemistry and real-time PCR analysis K. Tamakuma1, Y. Mizutani1, M. Ito1, K. Shiogama1, K. Inada1, K. Miyamoto2, H. Utsunomiya3, F. Mahara4 and Y. Tsutsumi1 1) Department of Pathology, Fujita Health University School of Medicine, Toyoake, 2) Department of Microbiology, 3) Division of Strategic Surveillance for Function Food and Comprehensive Traditional Medicine, Wakayama Medical University School of Medicine, Wakayama and 4) Mahara Clinic, Anan, Japan Abstract Japanese spotted fever (JSF) is caused by Rickettsia japonica, and lethal cases are reported yearly in southwest Japan. We thus established the method of diagnosing JSF by immunohistochemistry (IHC) and real-time PCR (RT-PCR) using formalin-fixed, paraffin-embedded skin biopsy specimens. Two monoclonal antibodies were used for IHC, and the 17k genus common antigen gene served as the target of RT-PCR. We collected skin biopsy (n = 61) and autopsy (n = 1) specimens from 50 patients clinically suspected of JSF. Immunohisto- chemically, the rickettsial antigens were localized as coarse dots in the cytoplasm of endothelial cells and macrophages. Thirty-one sero- positive cases plus one autopsy case (group A) and nine seronegative cases but with positive IHC and/or RT-PCR (group B) were judged as JSF. Nine cases were regarded as non-JSF disorders based on negative serology, IHC and RT-PCR (group C). Of 50 biopsies (eschar 34, eruptions 10, and scabs 6) from groups A and B, IHC and RT-PCR positivities were 94% (32/34) and 62% (21/34) for eschar, 80% (8/10) and 30% (3/10) for eruptions, and 33% (2/6) and 50% (3/6) for scabs. For IHC, eschar was most suitable, and scabs were insufficient. Unexpectedly, 18 biopsies happened to be fixed in 100% formalin, and this lowered the detection rate by RT-PCR, but IHC was tolerant. Sequence analysis using five skin biopsy specimens confirmed a 114 bp DNA stretch homologous to that reported for the target gene of R. japonica. In 26 (84%) of the 31 seropositive patients, the diagnosis was made by IHC and/or RT-PCR earlier than serology. Keywords: 17k genus common antigen, formalin-fixed paraffin-embedded specimen, immunohistochemistry, Japanese spotted fever, real-time PCR, Rickettsia japonica, skin biopsy Original Submission: 11 January 2011; Revised Submission: 16 April 2011; Accepted: 22 April 2011 Editor: D. Raoult Article published online: 7 May 2011 Clin Microbiol Infect 2012; 18: 260–267 10.1111/j.1469-0691.2011.03569.x confirmed [4,5]. Because fatal JSF cases have recently been Corresponding author: Y. Tsutsumi, MD, Department of seen in southwest Japan [6,7], establishment of reliable diag- Pathology, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192, Japan nostic assays is needed. E-mail: [email protected] Serological screening of IgM and IgG antibodies and detec- tion of Rj DNA in blood by polymerase chain reaction (PCR) are the main diagnostic tests for JSF [8,9]. Serology requires a minimal twofold increase of antibody titres between the initial Introduction and second blood samples. It usually takes a 2-week period; therefore this cannot be used in an emergency situation. There are two rickettsioses endemic in Japan: Japanese spot- Indeed, fatal JSF cases have occurred within 24 h of hospitaliza- ted fever (JSF) caused by Rickettsia japonica (Rj) and Tsutsuga- tion. Empirical treatment was started on clinical suspicion, and mushi disease caused by Orientia tsutsugamushi (Ot). JSF was serological diagnosis was made retrospectively [6]. first reported by Mahara, et al. [1,2] in 1984 in Tokushima, We have established diagnostic immunohistochemistry Shikoku Island. JSF is thus one of the newcomers to the (IHC) using two monoclonal antibodies in formalin-fixed, spotted fever group (SFG) rickettsioses [3]. In Japan, JSF paraffin-embedded (FFPE) specimens biopsied from eschar cases must be reported to the health authorities once and eruptions [10,11]. When tiny samples or superficial ª2011 The Authors Clinical Microbiology and Infection ª2011 European Society of Clinical Microbiology and Infectious Diseases CMI Tamakuma et al. Histopathological diagnosis of Japanese spotted fever 261 scabs were submitted, false-negative results happened. 5% fetal calf serum (Hyclone, Logan, UT, USA). The cells Therefore, we started detecting Rj DNA extracted from harvested 5 to 7 days after inoculation were fixed in 10% for- Ò FFPE skin biopsies with TaqMan real-time PCR (RT-PCR). malin overnight. Cell blocks of uninfected and infected L929 RT-PCR was targeted at the 17k genus common antigen cells were prepared by a gelation method using sodium algi- gene to yield short-length products. We utilized FFPE speci- nate membranes [13]. Cell blocks were also prepared from mens not only to establish histopathological diagnostic tools R. conorii (Malish strain)-infected monkey Vero cells (Fuller but also to avoid possible biohazard during handling of the Laboratories, Fullerton, CA, USA) fixed in 10% formalin. biopsy material. The aims of the present study are to establish the method Monoclonal antibodies and IHC for diagnosing JSF with IHC and RT-PCR in FFPE skin biop- Mouse IgM monoclonal antibodies, clones S3 and X1, directed sies, and to compare these two assays with serology. to the Rj Aoki strain were a gift from Dr Yosaburo Oikawa, Department of Parasitology, Kanazawa Medical University, Kanazawa. Both clones react with the epitope common to Materials and Methods SFG rickettsiae, but do not cross-react with Ot [14,15]. Sections, 4 lm thick, were prepared from cell blocks and Clinical specimens tissue specimens. After inactivating endogenous peroxidase In the period 2004–2010, we collected specimens from 50 with 0.3% H2O2 in methanol for 20 min, sections were heat- patients clinically suspected of having JSF. The clinics and retrieved in 10 mM citrate buffer, pH 7.0 for 10 min with a hospitals supplying samples included Mahara Clinic (Anan, pressure cooker. Incubation with the monoclonals (dilution: Tokushima, n = 17), Yamada Red Cross Hospital (Ise, Mie, 1:100) at room temperature overnight and then amino acid n = 13), Myojin Clinic (Kozagawa, Wakayama, n = 9), Uwaj- polymers (Simple Stain MAX-PO, Nichirei, Tokyo, Japan) for ima Municipal Hospital (Uwajima, Ehime, n = 7), Hyogo Pre- 30 min at room temperature followed [10,11]. Antigen local- fectural Awaji Hospital (Sumoto, Hyogo, n = 1), Shinano ization was visualized in 50 mM Tris–HCl buffer, pH 7.6 con- Hospital (Tomi, Nagano, n = 1), Yasu Hospital (Yasu, Shiga, taining 1 mM 3,3¢-diaminobenzidine and 0.006% H2O2. n = 1) and Notogawa Hospital (Higashiomi, Shiga, n = 1). Nuclei were counterstained with haematoxylin. Biopsy samples were taken from 49 cases, and autopsy material from one. The skin samples (n = 61) included eschar DNA preparation (n = 42), eruptions (n = 12) and scabs (n = 7). All but the Five 4-lm-thick FFPE sections were collected in Eppendorf’s autopsied tissues, fixed in formalin, were sent to our depart- tubes. After deparaffinization, DNA was extracted using a ment within 24–72 h. Normal skin sampled at autopsy QIAamp DNA FFPE Tissue kit (#56404; Qiagen, Hilden, served as a negative control. For serological assays, sera Germany). At sample processing, microtome blades were were sent to Ohara Research Laboratory, Fukushima, or renewed to prevent sample-to-sample contamination. Prefectural Institutes of Public Health. In total, 89 sera (acute 46 and convalescent 43) were analysed serologically, as Real-time PCR described earlier [12]. The cut-off value was set at <·40 for The 17k genus common antigen gene of SFG rickettsia origin both IgM and IgG. The Rj Aoki strain was used as the anti- was amplified by RT-PCR, according to the previous reports gen. Rickettsia was isolated in limited cases in Ohara [9,16,17]. Primer pairs for Rj consisted of 5¢-ATG AAT AAA Research Laboratory, as reported previously [12]. CAA GGT ACA GGA ACA-3¢ (forward: 24mer) and 5¢-AAG TAA TGC ACC TAC ACC TAC TC-3¢ (reverse: 23mer), gen- Cultivation of rickettsial strains and preparation of cell erating products of 114 bp length (GenBank D16515). Both blocks primers were 100% homologous to R. conorii (GenBank Rickettsiae (Aoki and Katayama strains of Rj and Kato, Karp M28480) and R. rickettsii (M28479), while three bases (for- and Gilliam strains of Ot) were sent from Ohara Research ward) and one base (reverse) were mismatched with R. typhi Laboratory. All strains were passed in cultured L929 cells (M28481) and R. prowazekii (M28482). Signals were detected Ò (fibroblast-like cells of a C3H/An mouse) at a biosafety level with a TaqMan hybridization probe FAM-GGT GGC GCA 3 containment laboratory in the Department of Microbiol- TTA CTT GGT TCT CAA TTC GGT AAG GG-TAMRA for ogy, Wakayama Medical University, Wakayama. Rj (Applied Biosystems, Foster City, CA, USA). The number of Ò The cells were grown at 32°Cin25cm2 plastic cell cul- bases mismatched with the TaqMan probe (35mer) was one ture flasks containing Dulbecco’s modified Eagle’s minimal base for R. conorii, two bases for R. rickettsii, three bases for essential medium (Nissui, Tokyo, Japan) supplemented with R. prowazekii and four bases for R. typhi. ª2011 The Authors Clinical Microbiology and Infection ª2011 European Society of Clinical Microbiology and Infectious Diseases, CMI, 18, 260–267 262 Clinical Microbiology and Infection, Volume 18 Number 3, March 2012 CMI Assays were carried out in 20 lL final volume containing to antibiotic therapy, and positivities of IHC and/or RT-PCR. 1.5–3.0 lL of sample DNA, 2· reaction mixture (10 lL, Pre- Case distribution in groups A and B (n = 41) is shown on mix Ex TaqÔ; TaKaRa Bio, Otsu, Shiga, Japan), 10 pmol prim- Japan’s map (Fig.
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